Intraperitoneal Heparin in Peritoneal Dialysis and Its Effect on Fibrinopeptide A in Plasma and Dialysate

Abstract

In 6 patients on continuous ambulatory peritoneal dialysis we investigated the inhibition of intraperitoneal fibrin formation by heparin. A continuous addition of 500 U of heparin per liter dialysate was used for 52 h. In plasma no heparin activity could be detected, even 52 h after intraperitoneal administration of heparin. The fibrin formation was determined by fibrinopeptide A, a thrombin-induced split product of fibrinogen. In patients under regular continuous ambulatory peritoneal dialysis we determined the fibrinopeptide A concentrations in plasma. The values were comparable with the fibrinopeptide A concentrations measured in disseminated intravascular coagulopathy. They decreased during intraperitoneal administration of heparin from 63.2 ± 11.8 to 4.9 ± 1.7 ng/ml. The fibrinopeptide A concentration in the 4-hour intraperitoneal dialysate (155.8 ± 15.7 ng/ml) decreased after heparin administration to 8.5 ± 2.0 ng/ml and was always higher than in plasma. We conclude that 500 U heparin per liter dialysate prevents the intraperitoneal fibrin formation. The low antithrombin III concentration (0.44 ± 0.13 mg/dl) in protein-poor dialysate seems to be sufficient to inhibit the thrombin activity after acceleration by heparin.

Intraperitoneal Heparin Ameliorates the Systemic Inflammatory Response in PD Patients

“…We have previously reported that the inhibition of factor Xa was unaffected by the intraperitoneal tinzaparin treatment [10]. Indeed, intraperitoneal heparins seem to have very limited effects on systemic haemostasis [18, 19]. It is of interest to note that the present study has demonstrated a pronounced local effect of intraperitoneal tinzaparin on both fibrinogen-fibrin turnover and inflammation, while the systemic effect was primarily linked to inflammation.…”

“…It is of interest to note that the present study has demonstrated a pronounced local effect of intraperitoneal tinzaparin on both fibrinogen-fibrin turnover and inflammation, while the systemic effect was primarily linked to inflammation. As intraperitoneal fibrinogen-fibrin turnover is a local phenomenon [19], these observations imply that the systemic inflammatory response could have become reduced secondary to the reduced intraperitoneal inflammation, i.e. that the systemic inflammatory response is affected by the intraperitoneal inflammation in PD patients.…”

Hypercoagulability and Secondary Hyperf ibrinolysis May Be Related to Abnormal Lipid Metabolism in Patients Treated with Continuous Ambulatory Peritoneal Dialysis

“…FPB p 15-42 and P-TG were all increased in CAPD patients compared with healthy individuals, while PT was shorter. In other studies [2,[21][22][23][24], FVII. TAT, protein S, fibrino gen. FPA.…”

“…Hypercoagulability and secondary hyperfibrinolysis have also been noted in CAPD patients [2,[20][21][22][23][24] although they do not require anticoagulants for extracor poreal circulation during dialysis and the mechanism involved is unclear. In recent years, it has become possible to measure many of the markers produced during coagu lation and fibrinolysis [4,5,25,26], In the present study, FIX.…”

When the color of peritoneal dialysis effluent can be used as a diagnostic tool

“…The main risk of fibrin overproduction is catheter obstruction. Intraperitoneal injection of unfractionated heparin (500 IU/L of dialysate) can prevent intraperitoneal fibrin formation without significant systemic anticoagulant effect and is recommended by some nephrology centers as long as the dialysate appears cloudy …”